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- Alzahraa Fergany
- Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan
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- Cai Zong
- Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan
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- Frederick Adams Ekuban
- Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan
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- Aina Suzuki
- Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan
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- Yusuke Kimura
- Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan
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- Sahoko Ichihara
- Department of Environmental and Preventive Medicine, Jichi Medical University School of Medicine , Shimotsuke, Japan
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- Yoichiro Iwakura
- Division of Experimental Animal Immunology, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Japan
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- Gaku Ichihara
- Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan
抄録
<jats:title>Abstract</jats:title> <jats:p>Acrylamide is a neurotoxicant in human and experimental animals. Interleukin-1β (IL-1β) is a proinflammatory cytokine known as a critical component of brain reaction to any insult or neurodegenerative pathologies, though its role in electrophile-induced neurotoxicity remains elusive. The aim of this study was to investigate the role of IL-1β in acrylamide-induced neurotoxicity in mice. Ten-week-old male wild-type and IL-1β knock-out mice were allocated into 3 groups each and exposed to acrylamide at 0, 12.5, 25 mg/kg body weight by oral gavage for 28 days. Compared with wild-type mice, the results showed a significant increase in landing foot spread test and a significant decrease in density of cortical noradrenergic axons in IL-1β KO mice exposed to acrylamide at 25 mg/kg body weight. Exposure to acrylamide at 25 mg/kg significantly increased cortical gene expression of Gclc, Gpx1, and Gpx4 in wild-type mice but decreased them in IL-1β KO mice. The same exposure level significantly increased total glutathione and oxidized glutathione (GSSG) in the cerebellum of wild-type mice but did not change total glutathione and decreased GSSG in the cerebellum of IL-1β KO mice. The basal level of malondialdehyde in the cerebellum was higher in IL-1β KO mice than in wild-type mice. The results suggest that IL-1β protects the mouse brain against acrylamide-induced neurotoxicity, probably through suppression of oxidative stress by glutathione synthesis and peroxidation. This unexpected result provides new insight on the protective role of IL-1β in acrylamide-induced neurotoxicity.</jats:p>
収録刊行物
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- Toxicological Sciences
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Toxicological Sciences 195 (2), 246-256, 2023-08-04
Oxford University Press (OUP)
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キーワード
詳細情報 詳細情報について
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- CRID
- 1360016870442958208
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- ISSN
- 10960929
- 10966080
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- データソース種別
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- Crossref